Mouse (Murine) GTPase NRas (NRAS) interaction partners

MEK1 (显示 MAP2K1 抗体) does not act as a general tumor suppressor in leukemogenesis. Rather, its effects strongly depend on the genetic context (RAS versus MYC (显示 MYC 抗体)-driven leukemia) and on the cell type involved.

our data indicate that endogenous NrasQ61R/+ induces an increase of Nras-GTP (显示 AK3 抗体) and cytokine-evoked signaling, which is intermediate between NrasG12D/+ and NrasG12D/G12D

loss of one allele of Hras (显示 HRAS 抗体) increased the sensitivity of mice to this carcinogen, and this effect was further exacerbated by the loss of the second Hras (显示 HRAS 抗体) allele. However, loss of one or both alleles of Nras failed to alter tumor burden, either in the absence or presence of Hras (显示 HRAS 抗体), after exposure to urethane.

a crucial role of RXRa in suppression of UVB-induced melanomas in the context of driver mutations such as activated CDK4(R24C/R24C) or oncogenic NRAS(Q61K) and altered expression of p53 and PTEN

Human GTPase NRas (NRAS) interaction partners

Mutation analysis Iindicate NRAS as the most commonly mutated gene in myeloma patients followed by KRAS ( and BRAF (显示 BRAF 抗体).

A rapid monophyletic evolution of melanoma subpopulations in response to targeted therapy that was not observed in non-targeted therapy was observed. NRAS mutations in BRAF (显示 BRAF 抗体) mutated patient treated with a BRAF (显示 BRAF 抗体) inhibitor were identified post-resistant samples. Sequence analysis showed that NRAS mutations co-occur with BRAF (显示 BRAF 抗体) mutations in single cells, and are not mutually exclusive.

studies suggest that ZDHHC9 (显示 ZDHHC9 抗体) may serve as a safe and effective target for developing therapies against NRAS-driven cancers

MEK1 (显示 MAP2K1 抗体) does not act as a general tumor suppressor in leukemogenesis. Rather, its effects strongly depend on the genetic context (RAS versus MYC (显示 MYC 抗体)-driven leukemia) and on the cell type involved.

NRAS was identified as a direct target of let-7e and promoted oncogenesis in glioma stem cells.

It may be that NRAS Q61R, found in around half of GCMNs,[9] is a less potent promoter of FGF23 (显示 FGF23 抗体) than the HRAS (显示 HRAS 抗体) mutations usually found in verrucous EN with CSHS, and requires a larger mutant clone to cause CSHS.

Zebrafish GTPase NRas (NRAS) interaction partners

Although oncogenic NRAS expression alone was found to be insufficient to promote tumor formation, loss of functional p53 (显示 TP53 抗体) was found to collaborate with NRAS expression in the genesis of melanoma.

GTPase NRas (NRAS) 抗原简介

Antigen Summary

This is an N-ras oncogene encoding a membrane protein that shuttles between the Golgi apparatus and the plasma membrane. This shuttling is regulated through palmitoylation and depalmitoylation by the ZDHHC9-GOLGA7 complex. The encoded protein, which has intrinsic GTPase activity, is activated by a guanine nucleotide-exchange factor and inactivated by a GTPase activating protein. Mutations in this gene have been associated with somatic rectal cancer, follicular thyroid cancer, autoimmune lymphoproliferative syndrome, Noonan syndrome, and juvenile myelomonocytic leukemia.